OBJECTIVE Human facial muscle activation underlies highly sophisticated signaling mechanisms that are critically important for healthy physiological function. Accordingly, the necessity to analyze facial muscle activation at high-resolution and in a non-invasive manner is important for the diagnosis and treatment of many medical conditions. However, current clinical examination methods are neither precise nor quantitative. APPROACH Wearable, multi-channel surface electromyography can provide a solution to this yet unmet challenge. Here, we present the design and testing of a customized surface electromyography electrode array for facial muscle mapping. MAIN RESULTS Muscle activation maps were derived from repeated voluntary facial muscle activations. A customized independent component analysis algorithm and a clustering algorithm were developed to identify consistent building block activation patterns within and between participants. Finally, focusing on spontaneous smile analysis and relying on the building block mapping, we classified muscle activation sources, revealing a consistent intra-subject activation and an inter-subject variability. SIGNIFICANCE The herein described approach can be readily used for automated and objective mapping of facial expressions in general and in the assessment of normal and abnormal smiling in particular.Cochlear ribbon synapses play a pivotal role in the prompt and precise acoustic signal transmission from inner hair cells (IHCs) to the spiral ganglion neurons, while noise and aging can damage ribbon synapses, resulting in sensorineural hearing loss. Recently, we described reduced fibroblast growth factor 22 (FGF22) and augmented myocyte enhancer factor 2D (MEF2D) in an ototoxicity mouse model with impaired ribbon synapses. Here, we investigated the mechanisms that underlie the FGF22/MEF2D- regulated impairment of ribbon synapses. We generated adeno-associated virus (AAV) carrying FGF22, shFGF22, MEF2D, shMEF2D, calcineurin (CalN), shCalN or corresponding scramble controls for transduction of cultured mouse hair cells. We found that FGF22 was a suppressor for MEF2D, but not vice versa. https://www.selleckchem.com/products/JNJ-26481585.html Moreover, FGF22 likely induced increases in the calcium influx into IHCs to activate CalN, which subsequently inhibited MEF2D. Cochlear infusion of AAV-shFGF22 activated MEF2D, reduced ribbon synapse number and impaired hearing function, which were all abolished by co-infusion of AAV-shMEF2D. Hence, our data suggest that the ribbon synapses may be regulated by FGF22/calcium/CalN/MEF2D signaling, which implied novel therapeutic targets for hearing loss.The highly organized laminar structure of the mammalian brain is dependent on successful neuronal migration, and migration deficits can cause lissencephaly and behavioral and cognitive defects. Here, we investigated the contribution of neuronal migration dysregulation to anesthesia-induced neurotoxicity in the fetal brain. Pregnant C57BL/6 mice at embryonic day 14.5 received 2.5% sevoflurane daily for two days. Cortical neuron migration and axon lengths were evaluated using GFP immunostaining. Morris water maze tests were performed to assess the effects of sevoflurane exposure on spatial memory in offspring. We found that sevoflurane exposure decreased axon length and caused cognitive defects in young mice. RNA sequencing revealed that these defects were associated with reduced neuro-oncological ventral antigen 2 (Nova2) expression. In utero electroporation experiments using Nova2 shRNA recapitulated this finding. Nova2 shRNA inhibited neuronal migration and decreased axon lengths. Finally, we found that Netrin-1/Deleted in Colorectal Cancer (Dcc) proteins acted downstream of Nova2 to suppresses neuronal migration. These findings describe a novel mechanism by which prenatal anesthesia exposure affects embryonic neural development and postnatal behavior.The Norway rat has important impacts on our life. They are amongst the most used research subjects, resulting in ground-breaking advances. At the same time, wild rats live in close association with us, leading to various adverse interactions. In face of this relevance, it is surprising how little is known about their natural behaviour. While recent laboratory studies revealed their complex social skills, little is known about their social behaviour in the wild. An integration of these different scientific approaches is crucial to understand their social life, which will enable us to design more valid research paradigms, develop more effective management strategies, and to provide better welfare standards. Hence, I first summarise the literature on their natural social behaviour. Second, I provide an overview of recent developments concerning their social cognition. Third, I illustrate why an integration of these areas would be beneficial to optimise our interactions with them. © 2020, Schweinfurth.The N-acyl amino acids are a family of bioactive lipids with pleiotropic physiologic functions, including in energy homeostasis. Their endogenous levels are regulated by an extracellular mammalian N-acyl amino acid synthase/hydrolase called PM20D1 (peptidase M20 domain containing 1). Using an activity-guided biochemical approach, we report the molecular identification of fatty acid amide hydrolase (FAAH) as a second intracellular N-acyl amino acid synthase/hydrolase. In vitro, FAAH exhibits a more restricted substrate scope compared to PM20D1. In mice, genetic ablation or selective pharmacological inhibition of FAAH bidirectionally dysregulates intracellular, but not circulating, N-acyl amino acids. Dual blockade of both PM20D1 and FAAH reveals a dramatic and non-additive biochemical engagement of these two enzymatic pathways. These data establish FAAH as a second intracellular pathway for N-acyl amino acid metabolism and underscore enzymatic division of labor as an enabling strategy for the regulation of a structurally diverse bioactive lipid family. © 2020, Kim et al.Surfactants possess the ability to reduce surface tension at low concentrations, resulting in emulsification, foaming, wetting, and solubilizing. As a versatile industrial material, surfactants can be widely used as additives in the industrial field as different as textile, metal processing, mineral processing, new materials, industrial cleaning, construction, and pharmaceuticals. The most extensive application of surfactants perhaps is in the household and cosmetic industries, such as laundry detergents, dishwashing detergents, facial and body cleansers, and preparation of emulsions and creams. However, the extensive use of detergents, cleaners, and cleansers on skin may cause itching, redness, and dryness termed as surfactant-induced irritation, which is at least, partially due to surfactant penetration into skin. To understand how surfactants penetrate into skin, this review summarizes the penetration models proposed by researchers in the past two decades, including the surfactant monomer penetration model, the surfactant micelle and submicelle penetration model, and the recently proposed surfactant charge density and penetration correlation model that demonstrates the correlation between the surfactant charge density and skin penetration.